Middle-aged  and elderly patients with cardiovascular disease (CVD) who have recovered from SARS-CoV-2 infection may experience depressive symptoms due to the physical and psychological impact of the pandemic.

To investigate the prevalence and predictors of depressive symptoms among the middle-aged and elderly with CVD who have recovered from SARS-CoV-2 infection in Wuhan, China, and to develop a prediction model for depressive symptoms.

A cross-sectional study was conducted among 462 former SARS-CoV-2 middle-aged and elderly patients with CVD in Jianghan District, Wuhan, China from June 10 to July 25, 2021. Depressive symptoms were assessed by the Patient Health Questionnaire-9 (PHQ-9). Potential predictors of depressive symptoms were selected by the least absolute shrinkage and selection operator (LASSO) regression. A prediction model was developed by random forest (RF) and logistic regression models and compared by the area under the receiver operating characteristic curve (AUROC). The discrimination, calibration, and practical utility of the prediction model were evaluated by the receiver operating characteristic (ROC) curve, calibration curve, and decision curve analysis (DCA). Bootstrap sampling was used for internal validation.

The prevalence of depressive symptoms among the participants was 35.93%. The prediction model included age, stethalgia after recovery, insomnia after recovery, post-traumatic stress disorder (PTSD), anxiety, fatigue, and perceived social support as predictors. The AUROC of the logistic regression model was 0.909 (95%CI: 0.879 ~ 0.939), indicating good discrimination. The calibration curve showed good calibration. The DCA showed that the prediction model had a net benefit for a wide range of risk thresholds. The internal validation confirmed the stability of the prediction model.

Depressive symptoms are common among middle-aged and elderly CVD patients who have recovered from SARS-CoV-2 infection in Wuhan, China. A prediction model with satisfactory performance was developed to estimate the risk of depressive symptoms among this population. Interventions targeting long COVID symptoms and social support should be considered to prevent depressive symptoms in CVD patients.

It remains unclear about the association between stroke and Coronavirus disease 2019 (COVID-19). Therefore, a Mendelian randomization (MR) analysis was conducted to explore the relationship between them.

In this study, the most recent large-scale genome-wide association studies (GWASs) were selected from the publicly available COVID-19 GWAS meta-analysis (Round 7) as the exposure. Data from a recent original stroke GWAS were used as the outcome for the experimental group, while the stroke GWAS data from the IEU GWAS database were used as the validation group. In addition, an MR analysis was conducted to explore the causal relationships of susceptibility, hospitalization, and severity of COVID-19 with stroke and its subtypes. In addition, the results of the experimental and validation groups were integrated to perform a meta-analysis.

The MR analysis results corroborated that there was a positively causal relationship between the hospitalization (OR, 1.11; p = 0.015) (ORmeta, 1.11; p < 0.001), and severity (OR, 1.06; p = 0.043) (ORmeta, 1.07; p = 0.002) of COVID-19 and cardioembolic stroke (CES). This result is supported by the validation group and sensitivity analysis.

This study demonstrates for the first time that COVID-19 hospitalization and COVID-19 severity are risk factors for CES.

Cytokine storm (CS) is a severe systemic inflammatory syndrome characterized by the excessive activation of immune cells and a significant increase in circulating levels of cytokines. This pathological process is implicated in the development of life-threatening conditions such as fulminant myocarditis (FM), acute respiratory distress syndrome (ARDS), primary or secondary hemophagocytic lymphohistiocytosis (HLH), cytokine release syndrome (CRS) associated with chimeric antigen receptor-modified T (CAR-T) therapy, and grade III to IV acute graft-versus-host disease following allogeneic hematopoietic stem cell transplantation. The significant involvement of the JAK-STAT pathway, Toll-like receptors, neutrophil extracellular traps, NLRP3 inflammasome, and other signaling pathways has been recognized in the pathogenesis of CS. Therapies targeting these pathways have been developed or are currently being investigated. While novel drugs have demonstrated promising therapeutic efficacy in mitigating CS, the overall mortality rate of CS resulting from underlying diseases remains high. In the clinical setting, the management of CS typically necessitates a multidisciplinary team strategy encompassing the removal of abnormal inflammatory or immune system activation, the preservation of vital organ function, the treatment of the underlying disease, and the provision of life supportive therapy. This review provides a comprehensive overview of the key signaling pathways and associated cytokines implicated in CS, elucidates the impact of dysregulated immune cell activation, and delineates the resultant organ injury associated with CS. In addition, we offer insights and current literature on the management of CS in cases of FM, ARDS, systemic inflammatory response syndrome, treatment-induced CRS, HLH, and other related conditions.

The Omicron subvariants of SARS-CoV-2 spread rapidly since 2021. Following China's relaxation of containment measures in December 2022, a surge in COVID-19 cases poses a public health threat. Early identification of elderly COVID-19 patients at death risk is crucial for optimizing treatment and resource use.

To develop a clinical score for predicting death risk in elderly COVID-19 patients at hospital admission, based on a cohort from the Second Hospital of Shandong University.

We established a retrospective cohort of hospitalized COVID-19 patients from November 1, 2022, to March 31, 2023. Cox regression identified prognostic factors, leading to the development of a nomogram-based prediction model and a clinical risk score. Patients were classified into low- and high-risk groups using optimal segmentation thresholds, with survival curves generated by the Kaplan-Meier method. An online risk calculator was developed to facilitate real-time risk assessment in clinical settings.

The cohort included 1413 hospitalized COVID-19 patients. Elderly patients (≥60 years, N = 971) had a high mortality rate of 18.13%. Four independent predictors of mortality were identified: age (HR = 1.07), serum albumin (HR = 0.88), serum potassium (HR = 0.35), and serum sodium (HR = 0.91). The developed risk score demonstrated strong predictive performance and effectively stratified patients into risk categories.

We developed a validated clinical risk score integrating age, serum albumin, potassium, and sodium levels to predict mortality in hospitalized elderly COVID-19 patients. This scoring system enables early risk stratification, assisting clinicians in decision-making and optimizing patient management.

Hypoalbuminemia is commonly observed in patients with severe Coronavirus Disease 2019 (COVID-19) and is independently associated with adverse outcomes. However, the efficacy of albumin administration on the clinical prognosis of these patients remains uncertain.

This multicenter retrospective study enrolled 458 patients with severe COVID-19 in four medical centers from December 1, 2022, to June 1, 2024. Clinical features and laboratory variables were collected through electronic medical records. The cohorts were divided into two groups: albumin administration and non-albumin administration. Propensity score matching (PSM) was used for minimizing confounding effect. Statistical analyses were conducted to assess the relationship between early albumin administration and 28-day mortality.

Four hundred and fifty-eight severe COVID-19 cases were included in the study, of which 167 (36.5%) received early albumin administration, while 291 (63.5%) did not. Among these patients, 140 experienced in-hospital mortality and 318 survived. Compared to survivors, non-survivors exhibited significantly lower serum albumin levels (29.1g/L vs.33.8g/L, p < 0.05). In comparison to patients with admission albumin levels ≥30 g/L, those with albumin levels <30 g/L had a significantly higher in-hospital mortality (48.4% vs 21.1%, p < 0.001). Prior to PSM, the albumin administration group demonstrated significantly higher 28-day and in-hospital cumulative survival rates compared to the non-albumin group (both p < 0.001). However, no significant differences were observed between the two groups following PSM (p = 0.21 and p = 0.41, respectively).

Hypoalbuminemia was correlated with adverse outcomes in severe COVID-19 patients. However, early albumin administration did not reduce 28-day mortality and in-hospital mortality in these patients, and more relative RCTs were required for validation.

The global pandemic of novel coronavirus pneumonia (COVID-19) has resulted in millions of deaths over the past three years. As one of the most commonly affected extra-pulmonary organs, numerous studies have reported varying degrees of liver injury in a significant proportion of patients with COVID-19, particularly in severe and critically ill patients. Early prediction of liver dysfunction in hospitalized patients would facilitate the clinical management of COVID-19 and improve clinical prognosis, but reliable and valid predictive models are still lacking.MethodsWe collected data from 286 patients with RT-PCR confirmed COVID-19 admitted to various ICUs from the case system. These patients were randomly divided into a training cohort (50%) and a validation cohort (50%). In the training cohort, we first used ROC curves to measure the predictive efficiency of each of the variables for the development of liver damage during hospitalization in patients with COVID-19, followed by LASSO regression analysis to screen the variables for predictive models and logistic regression analysis to identify relevant risk factors. A nomogram based on these variables was created following the above model. Finally, the efficiency of the prediction models in the training and validation cohorts was assessed using AUC, consistency index (C index), calibration curves and Decision Curve Analysis.ResultsOut of a total of 80 parameters for COVID-19 patients admitted to the ICUs, 10 were determined to be significantly associated with the occurrence of liver dysfunction during hospitalization. Based on these predictors, further prediction models were used to construct and develop a nomogram that was offered for practical clinical application. The C-index of the column line graphs for the training and validation cohorts was 0.956 and 0.844 respectively. in addition, the calibration curves for the model showed a high degree of agreement between the predicted and actual incidence of liver dysfunction in patients with COVID-19.ConclusionBy developing a predictive model and associated nomogram, we predicted the incidence of liver dysfunction during hospitalization in patients with COVID-19 in the ICU. The model's predictive performance was determined in both the training and validation cohorts, contributing to the clinical management of COVID-19.

Background: COVID-19 has largely become an endemic disease in many regions, with sporadic outbreaks, with some areas where the disease shows a seasonal pattern like the influenza virus. The focus has shifted towards managing mild and moderate forms of disease through outpatient care, aiming to prevent healthcare system overload. Consequently, identifying markers that could be used in stratifying the risk and the prognostic assessment has become crucial. Cardiovascular implications of COVID-19 are a critical area of research due to their significant impact on disease severity, mortality, and morbidity. Methods: We conducted a retrospective, observational study and included 472 patients, diagnosed with COVID-19, all of whom were admitted to Prof. Dr. Matei Bals National Institute of Infectious Disease, Bucharest, Romania. Levels of cardiac biomarkers like creatine kinase (CK), creatine kinase-myocardial band (CKMB), myoglobin, troponins, and NT-pro-BNP were measured and analyzed in relation to clinical presentation and outcomes. Results: We combined CKMB, myoglobin, and troponin I to predict hospital length of stay (LOS). Our model significantly predicted LOS (F = 12.537, p = 0.0001), with higher levels associated with prolonged stays (β = 0.166, p = 0.000). Logistic regression demonstrated that the combination of elevated CKMB and myoglobin levels significantly increased the odds of a longer LOS (OR = 1.679, p = 0.000). Furthermore, we found significant correlations with acute respiratory failure (p = 0.001), severe forms of disease (p = 0.000), and the development of complications during hospitalization (p = 0.027). Conclusions: These findings emphasize the value of combining cardiac biomarkers to stratify risk and predict hospital outcomes in COVID-19 patients. Routine cardiac monitoring and targeted management strategies could decrease the risk of complications, reducing the LOS. Our findings highlight the potential of cardiac biomarkers as prognostic tools to stratify risk, guide clinical interventions, and improve outcomes in COVID-19 patients.

As detailed in the first part of this review, post-infectious vasculitides are a wide and complex category, including several clinical, microbiological and neuroradiological patterns. In order to raise the suspicion for diagnosis, the knowledge of two different neuroradiological issues is needed, i.e. the knowledge of neuroimaging pattern of infections and the one of neuroimaging pattern of vasculitis.

The main aim of this second part is to summarize the neuroradiological features of post-infectious vasculitides focusing on imaging of vessels and consequences of vessel involvement, continuing the discussion proposed in the first part about neuroimaging of infections. In some cases, the two neuroradiological issues are both simultaneously present in the same patient, but in other cases only the second one can be depicted due to the latency between infection and vasculitis.

Beyond general features of cerebral vascular involvement in post-infectious vasculitides, some well-studied and homogenous diseases, as treponemal vasculitis, Varicella Zoster Virus (VZV) arteriopathy, neuroborreliosis, SARS-CoV2-related endotheliopathy are described in detail, being not rare and sometimes underdiagnosed. The main clinical and neuroradiological features of these conditions are deeply addressed, providing diagnostic clues and pictorial examples.

Although some general features are common in clinical presentation and neuroimaging of post-infectious vasculitides, there are few neuroimaging clues pointing out a specific microbial agent as causative. The main step is to raise the diagnostic suspicion in order to start the dedicated investigation pathway and treatment.

COVID-19 commonly leads to respiratory issues, yet numerous patients also exhibit a diverse range of neurological conditions, suggesting a detrimental impact of SARS-CoV-2 or the viral Spike protein on the central nervous system. Nonetheless, the molecular pathway behind neurological pathology and the presumed neurotropism of SARS-CoV-2 remains largely unexplored. We generated human cortical organoids (HCOs) derived from human induced pluripotent stem cells (hiPSC) to assess: (1) the expression of SARS-CoV-2 main entry factors; (2) their vulnerability to SARS-CoV-2 infection; and (3) the impact of SARS-CoV-2 infection and exposure to the Spike protein on their transcriptome. Results proved that (1) HCOs express the main SARS-CoV-2 receptors and co-receptors; (2) HCOs may be productively infected by SARS-CoV-2; (3) the viral particles released by SARS-CoV-2-infected HCOs are able to re-infect another cellular line; and (4) the infection resulted in the activation of apoptotic and stress pathways, along with inflammatory processes. Notably, these effects were recapitulated when HCOs were exposed to the Spike protein alone. The data obtained demonstrate that SARS-CoV-2 likely infects HCOs probably through the binding of ACE2, CD147, and NRP1 entry factors. Furthermore, exposure to the Spike protein alone proved sufficient to disrupt their homeostasis and induce neurotoxic effects, potentially contributing to the onset of long-COVID symptoms.

COVID-19 exhibits complex pathophysiological manifestations, characterized by significant clinical and biological heterogeneity. Identifying phenotypes may enhance our understanding of the disease's diverse trajectories, benefiting clinical practice and trials.

This study included adult patients with COVID-19 from Xinhua Hospital, affiliated with Shanghai Jiao Tong University School of Medicine, between December 15, 2022, and February 15, 2023. The k-prototypes clustering method was employed using 50 clinical variables to identify phenotypes. Machine learning algorithms were then applied to select key classifier variables for phenotype recognition.

A total of 1376 patients met the inclusion criteria. K-prototypes clustering revealed two distinct subphenotypes: Hypo-inflammatory subphenotype (824 [59.9%]) and Hyper-inflammatory subphenotype (552 [40.1%]). Patients in Hypo-inflammatory subphenotype were younger, predominantly female, with low mortality and shorter hospital stays. In contrast, Hyper-inflammatory subphenotype patients were older, predominantly male, exhibiting a hyperinflammatory state with higher mortality and rates of organ dysfunction. The AdaBoost model performed best for subphenotype prediction (Accuracy: 0.975, Precision: 0.968, Recall: 0.976, F1: 0.972, AUROC: 0.975). "CRP", "IL-2R", "D-dimer", "ST2", "BUN", "NT-proBNP", "neutrophil percentage", and "lymphocyte count" were identified as the top-ranked variables in the AdaBoost model.

This analysis identified two phenotypes based on COVID-19 symptoms and comorbidities. These phenotypes can be accurately recognized using machine learning models, with the AdaBoost model being optimal for predicting in-hospital mortality. The variables "CRP", "IL-2R", "D-dimer", "ST2", "BUN", "NT-proBNP", "neutrophil percentage", and "lymphocyte count" play a significant role in the prediction of subphenotypes. Use the identified subphenotypes for risk stratification in clinical practice. Hyper-inflammatory subphenotypes can be closely monitored, and preventive measures such as early admission to the intensive care unit or prophylactic anticoagulation can be taken.

Coronavirus disease 2019 (COVID-19) is a multi-system disease that can lead to various severe complications. Acute limb ischemia (ALI) has been increasingly recognized as a COVID-19-associated complication that often predicts a poor prognosis. However, the pathophysiology and molecular mechanisms underlying COVID-19-associated ALI remain poorly understood. Hypercoagulability and thrombosis are considered important mechanisms, but we also emphasize the roles of vasospasm, hypoxia, and acidosis in the pathogenesis of the disease. The angiotensin-converting enzyme 2 (ACE2) pathway, inflammation, and platelet activation may be important molecular mechanisms underlying these pathological changes induced by COVID-19. Furthermore, we discuss the hypotheses of risk factors for COVID-19-associated ALI from genetic, age, and gender perspectives based on our analysis of molecular mechanisms. Additionally, we summarize therapeutic approaches such as use of the interleukin-6 (IL-6) blocker tocilizumab, calcium channel blockers, and angiotensin-converting enzyme inhibitors, providing insights for the future treatment of coronavirus-associated limb ischemic diseases.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to evolve, potentially leading to variants of concern that could become more transmissible, resist treatment, evade host immunity and reduce the effectiveness of currently available vaccines. Improved vaccines are still required as vaccination remains the most effective strategy against this virus. We have produced two SARS-CoV-2 virus-like particles (VLPs) using a baculovirus BacMam expression platform and examined their immunogenicity in mice. VLP1 contains the spike protein from the Wuhan strain, whereas VLP2 contains that of an Omicron variant. Mice immunized with VLP1 and boosted with VLP2 developed significantly higher antibodies in the sera, as well as higher numbers of IFN-γ secreting cells than the control group. Furthermore, both VLPs induced virus-neutralizing antibodies against Wuhan and Omicron variants. In conclusion, VLPs have the potential for the development of a safe and effective vaccine against SARS-CoV-2 variants.

Viral infection by SARS-CoV2 is a pandemic affecting over 600 million people worldwide. One of five hospitalized patients may present myocardial injury, strongly associated with disease severity and mortality.

Retrospective cross-sectional study of hospitalized COVID-19 patients diagnosed between May 01, 2020, and June 30, 2021, from the database of the Registro Latinoamericano de Enfermedad Cardiovascular y COVID-19 (CARDIO COVID 19-20) with a troponin value recorded during hospitalization. A descriptive analysis of sociodemographic and clinical characteristics was performed. Bivariate analysis was conducted according to the presence or absence of myocardial injury. Survival analysis was made using Kaplan-Meier curves, by the presence of myocardial injury. A multivariate Poisson regression model was performed to determine factors associated with mortality. Statistical analyses were performed using the RStudio V.1.4.1717 package.

A total of 2,134 patients were included, 64.2% were male, and 911 patients had myocardial injury. The median age of the total population was 61 years. Individuals with myocardial injury had a higher prevalence of hypertension, diabetes, and dyslipidemia. Survival probability was lower in this subgroup. Patients with myocardial injury had a 1.95 times higher risk of death. Age, male sex, chronic kidney disease, arrhythmias, decompensated heart failure, requirement of inotropic/vasopressor, and invasive mechanical ventilation were related to higher mortality risk in patients with myocardial injury.

Patients with COVID-19 and myocardial injury exhibit a broad spectrum of cardiac abnormalities. Myocardial injury is associated with a higher disease severity and risk of in-hospital mortality. This multicenter study uniquely represents data from 13 Latin American countries, offering regional insights into the impact of myocardial injury during the COVID-19 pandemic.

Whether circulating testosterone, dihydrotestosterone, and estradiol levels or testosterone replacement therapy (TRT) affects the risk of COVID-19 and whether COVID-19 affects response to TRT remains unknown.

The study evaluated whether baseline testosterone, dihydrotestosterone, and estradiol levels or TRT are associated with risk of developing COVID-19 and whether COVID-19 affects treatment response to TRT.

Among 5204 men, aged 45 to 80 years, with hypogonadism in the TRAVERSE trial, 379 developed COVID-19. We compared baseline and on-treatment hormone levels, and safety and efficacy in participants with and without COVID-19 diagnosis.

Neither baseline nor on-treatment testosterone, estradiol, and dihydrotestosterone levels prior to COVID-19 differed significantly between men with and without COVID-19 diagnosis. Incidence of COVID-19 was similar in participants randomized to TRT or placebo groups (3-year Kaplan-Meier incidence 8.0% in TRT and 8.6% in placebo group, P = .823). Incidences of COVID-19-related hospitalizations (38.5% vs 32.8%, P = .222) and deaths (12.8% vs 8.9%, P = .247) were similar in the TRT and placebo groups. Changes in hypogonadal symptoms, libido, energy, and hemoglobin/hematocrit in response to TRT were attenuated in testosterone-treated men who developed COVID-19. Incidences of major adverse cardiovascular events, venous thromboembolism, and acute kidney injury were similar in those with COVID-19 diagnosis and those without.

In men with hypogonadism and cardiovascular disease (CVD) or increased risk of CVD, baseline and pre-COVID-19 on-treatment testosterone, dihydrotestosterone, and estradiol levels were similar in those who developed COVID-19 and those who did not. TRT did not affect the risk of COVID-19. COVID-19 attenuated the treatment response to TRT.

The COVIVAX study assessed the association between COVID-19 vaccination and the risk of common neurological disorders in a multicenter case-control design. Vaccination exposure was compared between individuals with a first diagnosis of a neurological disorder (cases) and age- and sex-matched controls. A total of 624 participants were enrolled, and after random 1:1 matching 265 cases and 265 matched controls (total 530 participants) were included in the analyses. The most frequent neurological diagnosis in cases were stroke (60.4%), multiple sclerosis (11.3%) and seizures (6.4%). The proportion of vaccinated participants was 72.1% among cases and 79.6% among controls. A protective role of vaccination on the risk of developing a new neurological disorder was detected in the unadjusted analysis (OR 0.50; 95% CI 0.29-0.86; p = 0.0114). After adjustment for confounders, the number of vaccination doses received was associated with a reduced risk of developing new neurological disorders for participants aged over 60 years ( p = 0.0472; OR 0.14, 95% CI 0.03-0.68), with pre-existing comorbidities (p = 0.0122; OR 0.04, 95% CI 0.01-0.99) and for stroke (p = 0.0232; OR 0.04, 95% CI 0.02-0.97). The COVIVAX study provided no warning sign regarding an increase in the risk of developing new neurological disorders following COVID-19 vaccination of any type or doses. A potentially protective effect of multiple doses of COVID-19 vaccines against the risk of stroke in people aged over 60 needs to be confirmed by further studies.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is common in children, and clinical manifestations can vary depending on age, underlying disease, and vaccination status. Most children will have asymptomatic or mild infection, but certain baseline characteristics can increase the risk of moderate to severe disease. The following article will provide an overview of the clinical manifestations of coronavirus disease 2019 in children, including the post-infectious phenomenon called multisystem inflammatory syndrome in children. Currently available treatment and prophylaxis strategies will be outlined, with the caveat that new therapeutics and clinical efficacy data are constantly on the horizon.

Cepharanthine (CEP) is a natural remedy that potently inhibits SARS-CoV-2 activity both in vitro and in vivo. To evaluate the efficacy and safety of CEP compared with placebo in adults with asymptomatic or mild coronavirus disease 2019 (COVID-19), we conducted a proof-of-concept, double-blind, randomized, placebo-controlled trial. Patients were randomized to receive 120 mg/day of CEP, 60 mg/day CEP or placebo for 5 days. Main outcome was the time from randomization to negative nasopharyngeal swab and safety. Among 262 randomized participants, 188 completed the trial among group of 120 mg/day CEP (n = 65), 60 mg/day CEP (n = 68) and placebo (n = 55). Neither 120 mg/day or 60 mg/day CEP shortened the time to negative significantly compared with placebo. However, 60 mg/day CEP showed a slight trend (difference=-0.77 days, hazard ratio (HR) = 1.40, 95% CI 0.97-2.01, p = 0.072). In analysis of participants with good medication compliance, 60 mg/day CEP significantly shortened the time to negative (difference=-0.87 days, HR = 1.56, 95% CI 1.03-2.37, p = 0.035). Adverse events were not different among the three groups, and no serious adverse events occurred. In conclusion, treatment of asymptomatic or mild Covid-19 with 120 mg/day or 60 mg/day did not shorten the time to negative significantly. However, 60 mg/day CEP showed a slight trend which needs future confirmatory trials to validate. (NCT05398705).

The type I interferon (IFN-I) response is a critical component of the immune defense against various viral pathogens, triggering the expression of hundreds of interferon-stimulated genes (ISGs). These ISGs encode proteins with diverse antiviral functions, targeting various stages of viral replication and restricting infection spread. Beyond their antiviral functions, ISGs and associated immune metabolites have emerged as promising broad-spectrum biomarkers that can differentiate viral infections from other conditions. This review provides an overview of the diagnostic potential of ISGs at transcript and protein levels, as well as their immune metabolites. We focus on their clinical applications and the sensitivity and specificity of these biomarkers through receiver operating characteristic (ROC) analysis. We highlight the need for further research to facilitate the effective translation of these biomarkers into clinical practice.

Myocardial injury is prevalent among patients hospitalized for COVID-19. However, the role of COVID-19 vaccines in modifying the risk of myocardial injury is unknown.

To assess the role of vaccines in modifying the risk of myocardial injury in COVID-19.

We enrolled COVID-19 patients admitted from March 2021 to February 2022 with known vaccination status and ≥1 assessment of hs-cTnI within 30 days from the admission. The primary endpoint was the occurrence of myocardial injury (hs-cTnI levels >99th percentile upper reference limit). A total of 1019 patients were included (mean age: 67.7 ± 14.8 years, 60.8% male, and 34.5% vaccinated against COVID-19). Myocardial injury occurred in 145 (14.2%) patients. At multivariate logistic regression analysis, advanced age, chronic kidney disease, and hypertension, but not vaccination status, were independent predictors of myocardial injury. In the analysis according to age tertiles distribution, myocardial injury occurred more frequently in the III tertile (≥76 years) compared with other tertiles (I tertile: ≤60 years; II tertile: 61-75 years) (P < 0.001). Moreover, in the III tertile, vaccination was protective against myocardial injury [odds ratio (OR): 0.57, 95% confidence interval (CI): 0.34-0.94; P = 0.03], while a previous history of coronary artery disease was an independent positive predictor. In contrast, in the I tertile, chronic kidney disease (OR: 6.94, 95% CI: 1.31-36.79, P = 0.02) and vaccination (OR: 4.44, 95% CI: 1.28-15.34, P = 0.02) were independent positive predictors of myocardial injury.

In patients ≥76 years, COVID-19 vaccines were protective for the occurrence of myocardial injury, while in patients ≤60 years, myocardial injury was associated with previous COVID-19 vaccination. Further studies are warranted to clarify the underlying mechanisms.

Electronic health records (EHRs) facilitate the accessibility and sharing of patient data among various health care providers, contributing to more coordinated and efficient care.

This study aimed to summarize the evolution of secondary use of EHRs and their interoperability in medical research over the past 25 years.

We conducted an extensive literature search in the PubMed, Scopus, and Web of Science databases using the keywords Electronic health record and Electronic medical record in the title or abstract and Medical research in all fields from 2000 to 2024. Specific terms were applied to different time periods.

The review yielded 2212 studies, all of which were then screened and processed in a structured manner. Of these 2212 studies, 2102 (93.03%) were included in the review analysis, of which 1079 (51.33%) studies were from 2000 to 2009, 582 (27.69%) were from 2010 to 2019, 251 (11.94%) were from 2020 to 2023, and 190 (9.04%) were from 2024.

The evolution of EHRs marks an important milestone in health care's journey toward integrating technology and medicine. From early documentation practices to the sophisticated use of artificial intelligence and big data analytics today, EHRs have become central to improving patient care, enhancing public health surveillance, and advancing medical research.

The molecular mechanisms regulating coronavirus pathogenesis are complex, including virus-host interactions associated with replication and innate immune control. However, some genetic and epigenetic conditions associated with comorbidities increase the risk of hospitalization and can prove fatal in infected patients. This systematic review will provide insight into host genetic and epigenetic factors that interfere with COVID-19 expression in light of available evidence.

This study conducted a systematic review to examine the genetic and epigenetic susceptibility to COVID-19 using a comprehensive approach. Through systematic searches and applying relevant keywords across prominent online databases, including Scopus, PubMed, Web of Science, and Science Direct, we compiled all pertinent papers and reports published in English between December 2019 and June 2023.

The findings reveal that the host's HLA genotype plays a substantial role in determining how viral protein antigens are showcased and the subsequent immune system reaction to these antigens. Within females, genes responsible for immune system regulation are found on the X chromosome, resulting in reduced viral load and inflammation levels when contrasted with males. Possessing blood group A may contribute to an increased susceptibility to contracting COVID-19 as well as a heightened risk of mortality associated with the disease. The capacity of SARS-CoV-2 involves inhibiting the antiviral interferon (IFN) reactions, resulting in uncontrolled viral multiplication.

There is a notable absence of research into the gender-related predisposition to infection, necessitating a thorough examination. According to the available literature, a significant portion of individuals affected by the ailment or displaying severe ramifications already had suppressed immune systems, categorizing them as a group with elevated risk.

The controversy surrounding the safety of coronavirus disease-19 vaccinations is part of a larger historical backdrop of ongoing discussions regarding vaccine safety that have spanned several decades. The historical disputes around measles, mumps, rubella, and influenza highlight the recurring pattern in which public doubt is fueled by false information and personal stories. A 2024 multinational study in the journal Vaccine presented preexisting safety indicators for myocarditis, pericarditis, Guillain - Barré syndrome, and cerebral venous sinus thrombosis. The study had a notably large sample size and contributed to the ongoing discussion of vaccine safety. Examining this research clarifies the subtle distinctions between demonstrating causality and simple association, emphasizing the importance of thorough scientific investigation and open communication. The following recommendations should be prioritized to tackle vaccine hesitancy and ensure that politicians, healthcare practitioners, and public health officials make informed decisions. Vaccine safety data should be openly and readily provided to the public, particularly regarding potential hazards and advantages. Establishing post-marketing surveillance systems to monitor and examine adverse effects linked to vaccinations helps strengthen public confidence in the safety monitoring process and officials' dedication to addressing safety concerns with thoroughness.

Hepatocellular carcinoma (HCC) patients with coronavirus disease 2019 (COVID-19) undergoing open surgery show increased adverse events (AEs) and mortality, while the safety of transarterial chemoembolization (TACE) in coinfected patients remains understudied, limiting available evidence. This study aims to investigate the safety of TACE in HCC patients coinfected with COVID-19, and to explore the potential risk factors affecting the occurrence of serious AEs (SAEs), thus providing evidence for clinical treatment strategies in such patients.

This retrospective study involved HCC patients who underwent TACE with or without COVID-19 infection at our institution from November 2022 to February 2023. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used for the diagnosis of COVID-19. Patients were divided into an infected group (diagnosed with COVID-19 within 2 weeks before or after the procedure) and an uninfected group (tested negative for COVID-19). SAEs were ascertained according to the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE) version 5.0. Logistic regression analysis of multiple clinical factors in preoperative baseline characteristics was performed to identify risk factors that might predict the occurrence of SAEs.

A total of 118 patients (73 in the infected group, 45 in the uninfected group) were included, of whom 83.9% were male (86.3% in the infected group vs. 80.0% in the uninfected group) and the median age was 55.9±12.4 years (56.8±12.3 vs. 54.5±12.7 years). The clinical spectrum of COVID-19 in the infected group were 80.8% mild, 13.7% moderate, 1.4% severe and 4.1% critical. Sixteen of the 118 patients experienced SAEs (19.2% vs. 4.4%, P=0.046). The predominant SAEs were respiratory system diseases (9.6% vs. 0.0%) and liver damage (2.7% vs. 2.2%). In the univariate analysis, infection status [odds ratio (OR): 5.102, P=0.04, 95% confidence interval (CI): 1.102-23.627], gender (OR: 2.857, P=0.09, 95% CI: 0.862-9.468), age (OR: 1.061, P=0.03, 95% CI: 1.007-1.118) and clinical spectrum of COVID-19 (OR: 4.259, P<0.001, 1.943-9.336) were considered as the potential risk factors of grade ≥3 AEs. In multivariate analysis, younger age (OR: 1.064, P=0.044, 95% CI: 1.002-1.131) and a milder clinical spectrum of COVID-19 (OR: 5.736, P=0.004, 95% CI: 1.772-18.568) were independent factors associated with a lower occurrence of SAEs.

TACE in HCC patients co-infected with COVID-19 was considered relatively safe. Age and clinical spectrum of COVID-19 were associated with SAEs in HCC patients treated with TACE.

Traditional Chinese medicine (TCM) has developed a rich theoretical system and practical experience in fighting to infectious diseases over the past thousands of years, and has played an important role in controlling the spread owing to its unique advantages. In particular, its significant contribution to the prevention and control of Corona Virus Disease 2019 (COVID-19) is widely recognized. COVID-19 infection is mainly non-severe with a favorable overall outcome, but patients with comorbidities tend to have a poor prognosis. However, a comprehensive review of TCM for preventing and treating COVID-19 with comorbidities across various systems is still lacking. Hence, this scoping review aims to conduct a comprehensive investigation on treatment outcome of TCM for treating COVID-19 with comorbidities across various systems.

The scoping review was conducted by searching English databases including PubMed and Web of Science, and Chinese databases including China National Knowledge Infrastructure and Wanfang between January 2020 and January 2024. We followed the inclusion and exclusion criteria to identify relevant literature. Information for inclusion in the literature were subsequently extracted and consolidated.

We enrolled 13 literature that met the inclusion criteria in the review finally. Our analysis revealed that research on COVID-19 with comorbidities was mostly focused on circulatory diseases, including hypertension, heart failure, and cerebrovascular diseases, most common comorbidities were hypertension. Followed by endocrine and metabolic diseases such as diabetes, respiratory diseases including pulmonary tuberculosis and chronic obstructive pulmonary disease have been also addressed. However, there were few studies on co-infectious urogenital system disease, and no studies on the rheumatic, immune, hematological, nervous, reproductive, and skin systems diseases. Based on existing studies, TCM has significantly improved the clinical symptoms of COVID-19 with comorbidities such as fever, fatigue, dry cough, anorexia and asthma, the absorption of lung lesions, shortened the duration of viral shedding and the course of disease.

TCM has great application prospects in treating COVID-19 with comorbidities. These findings could provide important evidence for clinicians to treat COVID-19 with comorbidities. Multi-center studies are required to confirm our results in the future.

To investigate the impact of SARS-CoV-2 infection on liver function and prognosis in patients with HBV infection.

A total of 154 HBV-positive patients (HBV ( +) group) and 154 HBV-negative patients (HBV (-) group) diagnosed with COVID-19 at Taizhou Hospital between December 10, 2022, and January 31, 2023, were included in this study. Clinical characteristics, treatment, and laboratory findings were collected from patients at three time points: before (T1), during (T2), and at the time of discharge (T3) from SARS-CoV-2 infection.

Compared to the HBV (-) group, the HBV ( +) group had a longer hospital stay (15 (9-22) days vs. 9 (5-16) days). Longitudinal comparisons of laboratory indicators from T1 to T3 showed a continuous decline in TP and ALB levels and a continuous increase in PT and TT levels in the HBV ( +) group. BUN levels increased during T2 and decreased thereafter. These differences were considered statistically significant (P < 0.05). Notably, the HBV ( +) group had a higher proportion of indicators elevated > 3 ULN from T1 to T2, including ALT (1.95%/5.19%), AST (3.25%/12.99%), ALP (1.95%/3.25%), GGT (4.55%/9.09%), TBIL (6.49%/9.09%), and DBIL (18.18%/22.73%). In the HBV (-) group, the elevations were mainly concentrated within 1-2 ULN, including AST (12.99%/22.08%), DBIL (10.39%/21.43%), BUN (12.99%/22.08%), CREA (20.13%/29.22%), and PLT (7.79%/14.94%). Furthermore, the incidence of liver injury from T1 to T3 was higher in the HBV ( +) group compared to the HBV (-) group (15.7% (20/127) vs. 7.2% (11/152), P < 0.05). Multivariate analysis showed that liver cirrhosis (HR = 4.847, 95% CI: 1.224-19.20, P = 0.025) and liver cancer (HR = 8.333, 95% CI: 2.156-32.209, P = 0.002) were independent risk factors for liver injury in the presence of SARS-CoV-2 infection.

SARS-CoV-2 infection has a higher proportion of liver injury in HBV-infected patients, affecting hepatic protein synthesis function. Those with cirrhosis and hepatocellular carcinoma are at higher risk of severe liver injury.

Background: Understanding the interactions between age and comorbidities is crucial for assessing COVID-19 mortality, particularly in patients with cardiac and pulmonary conditions. This study investigates the relationship between comorbidities and mortality outcomes in a cohort of hospitalized COVID-19 patients, emphasizing the interplay of age, cardiac, and pulmonary conditions. Methods: We analyzed a cohort of 3005 patients hospitalized with COVID-19 between 2020 and 2022. Key variables included age, comorbidities (diabetes, cardiac, pulmonary, and neoplasms), and clinical outcomes. Chi-square tests and logistic regression models were used to assess the association between comorbidities and mortality. Stratified analyses by age, diabetes, and pulmonary conditions were conducted to explore interaction effects. Additionally, interaction terms were included in multivariable logistic regression models to evaluate the combined impact of age, comorbidities, and mortality. Results: Cardiac conditions such as hypertension, ischemic cardiopathy, and myocardial infarction showed significant protective effects against mortality in younger patients and in those without pulmonary conditions (p < 0.001). However, these protective effects were diminished in older patients and those with pulmonary comorbidities. Age was found to be a significant modifier of the relationship between cardiac conditions and mortality, with a stronger protective effect observed in patients under the median age (p < 0.001). Pulmonary comorbidities significantly increased the risk of mortality, particularly when co-occurring with cardiac conditions (p < 0.001). Diabetes did not significantly modify the relationship between cardiac conditions and mortality. Conclusions: The findings highlight the complex interactions between age, cardiac conditions, and pulmonary conditions in predicting COVID-19 mortality. Younger patients with cardiac comorbidities show a protective effect against mortality, while pulmonary conditions increase mortality risk, especially in older patients. These insights suggest that individualized risk assessments incorporating age and comorbidities are essential for managing COVID-19 outcomes.

While acute cardiovascular complications of coronavirus disease 2019 (COVID-19) are well described, less is known about longer-term cardiac sequelae. For many individuals with cardiac signs or symptoms arising after COVID-19 infection, the aetiology remains unclear. We examined immune profiles associated with magnetic resonance imaging (MRI) abnormalities in patients with unexplained cardiac injury after COVID-19.

Twenty-one participants {mean age 47 [standard deviation (SD) 13] years, 71% female} with long COVID-19 (n = 17), raised troponin (n = 2), or unexplained new-onset heart failure (n = 2), who did not have pre-existing heart conditions or recent steroid/immunosuppression treatment, were enrolled a mean 346 (SD 191) days after COVID-19 infection in a prospective observational study. Cardiac MRI and blood sampling for deep immunophenotyping using mass cytometry by time of flight and measurement of proteomic inflammatory markers were performed. Nine of the 21 (43%) participants had MRI abnormalities (MRI(+)), including non-ischaemic patterns of late gadolinium enhancement and/or visually overt myocardial oedema in 8 people. One patient had mildly impaired biventricular function without fibrosis or oedema, and two had severe left ventricular (LV) impairment. MRI(+) individuals had higher blood CCL3, CCL7, FGF-23, and CD4 Th2 cells, and lower CD8 T effector memory (TEM) cells, than MRI(-). Cluster analysis revealed lower expression of inhibitory receptors PD1 and TIM3 in CD8 TEM cells from MRI(+) patients than MRI(-) patients, and functional studies of CD8 T αβ cells showed higher proportions of cytotoxic granzyme B+(GZB+)-secreting cells upon stimulation. CD8 TEM cells and CCL7 were the strongest predictors of MRI abnormalities in a least absolute shrinkage and selection operator regression model (composite area under the curve 0.96, 95% confidence interval 0.88-1.0). CCL7 was correlated with diffuse myocardial fibrosis/oedema detected by quantitative T1 mapping (r = 0.47, P = 0.04).

COVID-19-related cardiac injury in symptomatic patients with non-ischaemic myocarditis-like MRI abnormalities is associated with immune dysregulation, including decreased peripheral CD8 TEM cells and increased CCL7, persisting long after the initial infection.

The COVID-19 outbreak, caused by the SARS-CoV-2 virus, was linked to significant neurological and psychiatric manifestations. This review examines the physiopathological mechanisms underlying these neuropsychiatric outcomes and discusses current management strategies. Primarily a respiratory disease, COVID-19 frequently leads to neurological issues, including cephalalgia and migraines, loss of sensory perception, cerebrovascular accidents, and neurological impairment such as encephalopathy. Lasting neuropsychological effects have also been recorded in individuals following SARS-CoV-2 infection. These include anxiety, depression, and cognitive dysfunction, suggesting a lasting impact on mental health. The neuroinvasive potential of the virus, inflammatory responses, and the role of angiotensin-converting enzyme 2 (ACE2) in neuroinflammation are critical factors in neuropsychiatric COVID-19 manifestations. In addition, the review highlights the importance of monitoring biomarkers to assess Central Nervous System (CNS) involvement. Management strategies for these neuropsychiatric conditions include supportive therapy, antiepileptic drugs, antithrombotic therapy, and psychotropic drugs, emphasizing the need for a multidisciplinary approach. Understanding the long-term neuropsychiatric implications of COVID-19 is essential for developing effective treatment protocols and improving patient outcomes.

COVID-19 disease has spread rapidly worldwide, causing high mortality. Accessible biomarkers capable of early identification of patients at risk of severe form are needed in clinical practice. The aim of the study was to determine the biological markers that predict a critical condition.

Retrospective study including patients with confirmed COVID-19 hospitalized between September 2020 and June 2021. The primary endpoint was progression to critical status within 7 days from admission. We defined two groups:Critical group: Patients who developed a critical condition or died or transferred to the ICU before or at 7 th day.Non-critical group: Patients who remained in non-critical respiratory status until 7 th day or discharged before or at 7 th day.

Our study included 456 patients, with a sex ratio of 1.32 and an average age of 62 years. At the 7 th day of hospitalization, 115 (25.2%) patients were in the critical group and 341 (74.8%) patients were in the non-critical group. The univariate logistic regression indicated that laboratory findings between non-critical and critical groups showed that C-reactive protein (CRP) (p=0.047), D-Dimer (p=0.011), creatinine (0.026), creatine kinase (p=0.039), lactate dehydrogenase (p=0.04), and troponin (p=0.001) were all higher among patients in critical group. However, lymphocyte (p<0.001) and platelet (p<0.001) counts were significantly lower among the critical group. Multivariate logistic regression model, identified four independent risk factors: lymphopenia (OR=2.771, 95%CI=1.482-5.181, p=0.001), Neutrophil to Lymphocyte Ratio (NLR) (OR=2.286, 95%CI=1.461-3.578, p<0.001), thrombocytopenia (OR=1.944, 95%CI=1.092-3.459, p=0.024), and CRP>71.5 (OR=1.598, 95% CI=1.042-2.45, p=0.032) were associated to critical group.

Our results show the predictive value of lymphopenia, thrombocytopenia, high NLR and CRP levels to evaluate the prognosis of COVID-19 pneumonia. A prognostic score could be proposed for guiding clinical care and improving patient outcomes.